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Received July 9, 2003
Revised August 21, 2003
Accepted after revision December 19, 2003
1 University of Rochester
2 University of Rochester Medical Center
* To whom correspondence should be addressed. E-mail: ingrid_sarelius{at}urmc.rochester.edu.
We addressed the role of endothelial cells (ECs) in metabolic dilatation of skeletal muscle arterioles in anesthetized mice in situ. Electrical field stimulation was used to contract the cremaster muscle for 15 seconds at 30 Hz. Diameter was observed using bright field microscopy. Muscle contraction produced a 15.7±1.5 µm dilatation (in controls) from a baseline of 17.4±1.6 µm. Endothelial denudation via intraluminal perfusion of air abolished this response (1.6±1.2 µm in -EC, P<0.05), identifying endothelium as the primary vascular cell type initiating the dilatation. To investigate the role of EC Ca2+ in metabolic dilatation, ECs of arterioles were loaded with Fluo-4 (AM) or BAPTA (AM) by intraluminal perfusion after which blood flow was reestablished. Ca2+ activity of individual ECs was monitored as a function of change from baseline using confocal microscopy. In ECs, whole cell Ca2+ increased (> 10%, P<0.05) during muscle contraction and localized Ca2+ transients were increased (>20%, P<0.05) during the first minute after contraction. Chelation of EC Ca2+ abolished the dilatations to muscle contraction (1.1±0.7 µm, P<0.05). Inhibition of P1 purinergic receptors (with xanthine amine congener) did not alter the rate of onset of the dilatation (P>0.05) but decreased its magnitude immediately post stimulation and during recovery (7.1±0.9 µm, P<0.05). These findings demonstrate obligatory roles for endothelium and EC Ca2+ during metabolic dilatation in intact arterioles. Furthermore, they indicate that at least two separate pathways mediate the local response, one of which involves stimulation of endothelial P1 purinergic receptors via endogenous adenosine produced during muscle activity.
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